Neuropathy and Spinal Cord Stimulation (“SCS”)
Neuropathic pain is prevalent in the US in approximately 1.5% of the population, 1% in the UK, and at a comparable level in Canada (“Spinal Cord Stimulation for Neuropathic Pain, Health Technology Literature Review,” Ministry of Health and Long Term Care, Toronto, Ontario, Canada, 2005). In 2002, it was reported that between 6 and 10 million Americans were afflicted with Neuropathic pain (P. S. Staats, “Intrathecal Therapy for Neuropathic Pain,” Proceedings of the 18th Annual Meeting of the American Academy of pain Medicine (AAPM), San Francisco, 2002). Neuropathic pain is generally caused by a dysfunction in the nervous system and is a known complication of diabetes mellitus, which represents 6% of the US population. About 15 percent of patients with diabetes have both symptoms and signs of neuropathy, but nearly 50 percent have evidence of peripheral nerve damage as judged by nerve conduction abnormalities (A. H. Ropper, R. H. Brown, ADAMS AND VICTOR'S PRINCIPLES OF NEUROLOGY, Eighth Edition, The McGraw-Hill Companies, Inc, 2005, ch.46). People suffering from neuropathic pain are generally considered to have chronic pain, which can lead to loss of productivity, depression and reduction in Quality of Life. Neuropathy presents as Failed Back Surgery Syndrome (FBSS), Complex Regional Pain Syndrome (CRPS), and postherpetic neuralgia. For each of these conditions, Spinal Cord Stimulation (SCS) is considered as a viable therapy only after failure of treatments with pharmacological, nonpharmacological and surgical treatments.
SCS systems are comprised of an implantable pulse generator and a lead with electrodes at the distal end surgically positioned in the epidural space, posterior to the spinal cord. SCS treatment is considered weakly to moderately effective in the treatment of chronic pain due to neuropathy when all else fails. SCS works by passing impulses through a nerve fiber that is either inhibiting the pain signal, or disrupting a nerve fiber that is conducting the pain signal.
SCS Limitations
For patients studied between 2000 and 2005, about 1.2% had complication due to infection and another 1.2% due to dural puncture and 11% technical failures due to electrode migration or malpositioning. Additionally, SCS electrodes used to be implanted in a less conductive medium than that of the Cerebral Spinal Fluid (CSF), percutaneously, but complications with fibrosis altered device behavior (K. M. Alo, “Recent Advances in Neurostimulation Analgesia,” Techniques in Regional Anesthesia and Pain Management, Vol. 5, No. 4, 2001, pp: 142-151). Since the CSF is highly conductive, it acts as a shunt, requiring electrode guarding techniques and increase in number of stimulation sites to four in order to obtain adequate current focusing. This approach is highly sensitive to electrode placement due to the need to focus the electric current across the stimulated axon, and over time, the electrodes migrate in the epidural space, decreasing the effectiveness of the treatment.
Nociceptive Pain
More generally, chronic pain (CP) that is nociceptive has been poorly defined and documented until recently and is considered widely undertreated. According to the International Association for the Study of Pain (IASP), CP prevalence ranges from 10.5% to 55.2%. The American College of Rheumatology (ACR) estimated CP prevalence at 10.1% to 13%. Studies show that there is little variation of prevalence in populations, ranging from 8% in children to approximately 11% in Adults. CP is generally defined as pain that persists beyond the normal time of healing and may be associated with a disease where healing may never occur (M. Ospina and C. Harstall, “Prevalence of Chronic Pain: An Overview,” Alberta Heritage Foundation for Medical Research, Health Technology Assessment, Edmonton, Alberta, Canada, (2002)). Different associations have generally defined CP to present as chronic if it persists beyond the range of one to six months, with many agreeing on three.
Treatment of nociceptive pain that is acute, post-surgical or chronic is generally done with analgesics. In particular, chronic pain has given rise to patient-controlled-analgesic infusion pumps (PCA's) (see U.S. Pat. No. 5,630,710), which are capped to limit amount of opiates and reduce dependency. In addition, transcutaneous electrical neural stimulators (TENS) devices (see, e.g., U.S. Pat. No. 4,121,594) demonstrated moderate impact on the suppression of pain, but were never used alone to suppress severe pain. Many TENS devices are commonly used for massage, where they pass electrical current through large muscle fiber, contracting it and in essence stimulating ascending large fiber neurons which were thought to suppress pain. SCS devices are deployed when all pharmacological solutions are exhausted in patients with intractable pain. Studies have also shown that intermittent stimulation of the spinal cord in sessions provides relief for both nociceptive and neuropathic pain, allowing of the scheduling of stimulation sessions using non-implantable subcutaneous needle electrodes.
Mechanisms of Pain
Pain, whether introduced nociceptively by tissue damage, or neuropathically by nerve damage, is conducted through the peripheral nervous system and transmitted to the spinal cord via Aδ and C-fibers. C fibers are small, non-myelenated and slow conducting in the range of 0.5-1.2 m/s. C-fiber diameter is in the order of 1 mm and has a membrane time constant of 0.25-3 ms. Some Aδ fibers are faster conducting 12-36 m/s and have membrane time constants that range to 0.1 ms (L. R. Squire, F. E. Bloom, S. K. McConnell, J. L. Roberts, N. C. Spitzer, M. J. Zigmond, Fundamental Neuroscience, Second Edition, Academic Press, Elsevier Science, San Diego Calif., 2003, ch. 25).
Aδ fibers, the faster conductors of pain, are carriers of the “first pain” sensation that is very highly localized. First pain is much more tolerable than the sustained second pain, and is the trigger to a reflexive withdrawal to cutaneous pricking, for instance. Aδ fibers are also mechanoceptors that respond to application of heat with very high threshold. Repeated application of heat stimuli on Aδ mechanoceptors receptor sites decreases the threshold, increases the response, thus leading to sensitization.
C fibers are polymodal, responding to tissue deformation, noxious stimuli and heat. They are responsible for the second pain which is poorly localized and poorly tolerated. In general, they transmit burning sensations. Aβ fibers are larger mechanoceptors, synapsing more anteriorally within the spinal cord to Aδ and C fibers. These larger fibers are considered by some researchers to be responsible for the “Gate Control Theory,” where their stimulation is responsible for neuromodulation, or suppression, of pain sensation in the smaller fiber group. Many have refuted this finding, yet it is known that muscle contraction of pain-sites using TENS devices decreases pain response and provides prolonged relief.
Neuromagnetic Stimulation
Devices and methods for performing neurostimulation using a combination of a magnetic field and ultrasound have been described. See., e.g., U.S. Pat. No. 5,476,438. Such systems purport to stimulate nerves by applying a magnetic field generally to the nerve and simultaneously focusing an ultrasound beam on the nerve.